th

4 SymCARD 2014

Up Date on
Acute Coronary Syndrome
Management
 Pendahuluan
• Sindrom Koroner Akut (SKA) Meningkatkan angka perawatan
dan Kematian di seluruh dunia
• Saat ini Penanganan SKA sudah mengalami banyak kemajuan
dibanding 2 dekade terakhir

Marso SP, et al. Comparison of Myocardial Reperfusion in Patients Undergoing Percutaneous Coronary
Intervention in ST-Segment Elevation Acute Myocardial Infarction With Versus Without Diabetes
Mellitus. Am J Cardiol 2007;100: 206-210
4 thSymCARD 2014 2
 Klasifikasi SKA

ESC Guidelines for the management of Acute Coronary Syndrome in patients without
persistent ST Elevation.2011
 Nyeri Dada Khas Infark

• Nyeri dada Angina Saat Istirahat (>20 Menit)

• Nyeri dada angina Pertama Kali (de Nuvo) dengan
tingkatan CCS III
• Cresendo Angina
• Angina Paska Infark
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 Elektrokardiografi

 The most important

 Serial EKG is routinely
 Classify ACS
 Determine severity and prognosis

4 thSymCARD 2014
  Elevasi Segmen ST pada J Point pada 2 lead yg berhubungan
 ≥0.25 mV Pada laki-laki dibawah 40th
STEMI  ≥0.2 mV pada laki-laki diatas 40th, or ≥0.15 mV pada wanita di
lead V2–V3 dan/atau ≥0.1 mV pada lead lainnya

Depresi Segmen ST horizontal/downsloping baru ≥ 0.1 mV pada 2 lead

NSTEMI/UAP yg berhubungan
T Inverted ≥ 0.1 mV

ESC Guidelines for the management of acute myocardial infarction in patients presenting
with ST-segment elevation. 2011. 4 thSymCARD 2014
 Marka Jantung

• Pada pasien dg SKA Peningkatan

enzinm Troponin terjadi 4 jam
setelah onset gejala
• Troponin dapat bertahan selama 2
minggu didalam darah
• Pemeriksaan serial harus dilakukan
dlm 6-12 jam jika pemeriksaan
pertama negatifPemeriksaan
CKMB atau Troponin T sangat
bermanfaat utk mendiagnosis SKA

ESC Guidelines for the management of Acute Coronary Syndrome in patients without
persistent ST Elevation.2012
Angiography Coroner

4 thSymCARD 2014
Bagaimana Penanganan SKA?

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Tindakan Umum & Langkah Awal

2
Suplemen Oksigen diberikan utk semua SKA dlm 6 jam pertama tanpa mempertimbangkan
Saturasi (IIa-C)

4 Aspirin tanpa salut 160-320 mg pd semua ps yg toleran thdp Aspirin (I-C)

5
Anti Iskemik: NTG spray/tab (I-C), Morfin sulfat 1-5 mg IV dpt diulang setiap 10-30 menit (IIa-B)
5
4 thSymCARD 2014 10

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Persangkaan SKA

Non Kardiak Angina Stabil (Kronik) Kemungkinan Definitif SKA

SKA

Elevasi segemen ST (STEMI)

• EKG: Normal atau
nondiagnostik
• Marka Jantung awal:
Normal
Observasi 12 jam setelah
awitan Angina
• Angina tdk berulang • Angina berulang,atau
• EKG:tdk berubah • EKG: perubahan ST
• Marka jantung:Normal dan/atau gelombang T
• Marka Jantung : positif
Tanpa Elevasi segmen ST
atau LBBB Baru
• Perubahan ST dan/atau
• Gelombang T
• Angina berlanjut
• Marka Jantung Positif
• Hemodinamik abnormal
Definitif SKA Evaluasi terapi reperfusi

NEGATIF POSITIF
Diagnostik: Bukan SKA atau Diagnosis: Definitif atau sangat Terapi NSTEMI
Resiko rendah SKA mungkin SKA

Pemantauan rawat Jalan

Algoritma evaluasi dan tatalaksana SKA

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi Reperfusi pada STEMI

4 thSymCARD 2014
*Patients with cardiogenic shock or severe heart failure initially seen at a non–PCI-capable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time
delay from MI onset (Class I, LOE: B). †Angiography and revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy.
DIDO = door-in-door-out
Jika Waktu yang dibutuhkan untuk
mecapai RS dg Fasilitas PCI > 2jam 
Lakukan Fibrinolitik Di RS anda !

4 thSymCARD 2014
 Kontra Indikasi Fibrinolitik
Kontraindikasi Absolut Kontraindikasi Relatif
Stroke hemoragik atau stroke yg Transient Ischaemic Attact(TIA) dlm 6
penyebabnya blm diketahui dg awitan bulan terakhir
kapanpun
Stroke iskemik 6 bulan terakhir Pemakaian antikoagulan oral
Kerusakan sistem syaraf sentral dan Kehamilan atau dalam 1 minggu post-
neoplasma partum
Trauma operasi/trauma kepala yg berat Resusitasi traumatik
dalam 3 minggu terakhir
Penyakit perdarahan Hipertensi refrakter (TDS >180 mmHg)
Diseksi aorta Penyakit hati lanjut
Infeksi endokartis
Ultus peptikum yang aktif

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
Regimen Fibrinolitik untuk Infark Miokard Akut
Agen Dosis Awal Ko Terapi Kontraindikasi spesifik
Antitrombotik
Streptokinase (Sk) 1,5 juta U dalam 100 ml Heparin iv selama 24-48 Sebelum SK atau
dextrose 5% atau dlm jam Anistreptase
larutan salin 0,9% dlm
30-60 menit
Alteplase (tPA) Bolus 15mg IV Heparin IV selama 24-48
0,75 mg/kg selama 30 jam
menit, kemudian 0,5
mg/kg selama 60 mrnit
Dosis total tidak lebih
dari 100 mg

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi NSTEMI

4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
 Terapi Reperfusi pada NSTEMI
Rekomendasi Kelas rekomendasi Level
Urgent PCI (<2 jam) Angiography segera I C
dilakukan (<2 jam) pd
pasien dengan:
Angina refrakter
Gagal Jantung
Aritmia ventrikel yg
mengancam
Hemodinamik tdk stabil
Pada pasien dengan Skor I A
Early Invasive GRACE > 140 atau dengan
(<24 jam) paling tidak 1 kriteria
resiko tinggi
Invasive Strategy 1 kriteria resiko tinggi I A
Gejala rekuren
(72 jam setelah
presentasi)
4 thSymCARD 2014
Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014
Grace Score

4 thSymCARD 2014
 SKA

Mencegah
Trombosis Lebih
Resiko
Lanjut Perdarahan↑

Prognosis Baik Prognosis Buruk 4 thSymCARD 2014

Hubungan Perdarahan dengan Angka Kematian

4 thSymCARD 2014
20,078 Patients

12,092 Patients

4 thSymCARD 2014
 Fondaparinux Significantly Reduced Mortality vs. Enoxaparin
up to Day 30
0.04

Enoxaparin
0.03
Cumulative Hazard

Fondaparinux
0.02

0.01
HR: 0.83
95% CI: 0.71-0.97
p=0.02
0.0

0 3 6 9 12 15 18 21 24 27 30
Days
4 thSymCARD 2014
1. ArixtraTM PI BPOM GDS04/IPI04 (23 January 2007).
1. Salim Yusuf, et al. Comparison of Fondaparinux and Enoxaprine in Acute Coronary Syndrome.
The fifth organization to assess strategies in Acute Ischemic Syndrome investigator. N Egl J Med 2006:354:1446-76.
 Fondaparinux Reduced the Rate of the Composite of Death, MI or
Stroke up to 6 Months

0.14

0.12 Enoxaparin

Cumulative Hazard 0.10 Fondaparinux

0.08

0.06

0.04
HR: 0.89
0.02 95% CI: 0.82-0.97
p=0.007
0.0
0 20 40 60 80 100 120 140 160 180
Days
1. ArixtraTM PI BPOM GDS04/IPI04 (23 January 2007).
1. Salim Yusuf, et al. Comparison of Fondaparinux and Enoxaprine in Acute Coronary Syndrome.
The fifth organization to assess strategies in Acute Ischemic Syndrome investigator. N Egl J Med 2006:354:1446-76.
Fondaparinux Patients Experienced Half the Rate of Major Bleeding Than
Enoxaparin Patients at Day 9 (Primary Safety)

0.04 Enoxaparin
HR: 0.52
95% CI: 0.44-0.61 p<0.001
0.03
Cumulative Hazard

0.02

Fondaparinux
0.01

0.0

0 1 2 3 4 5 6 7 8 9
Days
4 thSymCARD 2014
1. ArixtraTM PI BPOM GDS04/IPI04 (23 January 2007).
1. Salim Yusuf, et al. Comparison of Fondaparinux and Enoxaprine in Acute Coronary Syndrome.
The fifth organization to assess strategies in Acute Ischemic Syndrome investigator. N Egl J Med 2006:354:1446-76.
 Kesimpulan
• SKA merupakan merupakan penyebab utama kematian mendadak di dunia
• Diagnosis dan tatalaksana meliputi, Pemberian antiplatelet, anti iskemik,
antikoagulan, statin dan Ace inhibitor, Terapi Revaskularisasi (PCI atau
Fibrinolitik) untuk STEMI
• Perdarahan Merupakan resiko yg mungkin tjd selama terapi SKA
• Fundaparinuk Secara keseluruhan memiliki profil keamanan berbanding
risiko yg paling baik (Kelas I-A)

4 thSymCARD 2014
Terimakasih

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Normal QRS complexes
•ST segment depression -
horizontal in leads
•V3-V4, downward-sloping in leads
I, VL, V5-V6

Clinical interpretation
•This ECG shows anterior and
lateral ischaemia without evidence
of infarction.
•Taken with the clinical history, the
diagnosis is clearly 'unstable‘
angina.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Small Q waves in leads II, III, VF
•Biphasic T waves in leads II, V6;
inverted T waves in leads III, VF
•Markedly peaked T waves in leads
V1-V2

Clinical interpretation
•The Q waves in the inferior leads,
together with inverted T waves,
point to an old inferior myocardial
infarction.
•While symmetrically peaked T
waves in the anterior leads can be
due to hyperkalaemia, or to
ischaemia, they are frequently a
normal variant

4 thSymCARD 2014
The ECG shows:
•Complete heart block
•Ventricular rate 45/min
Clinical interpretation
•In complete heart block there is
no relationship between the P
waves (here with a rate of 70/min)
and the QRS complexes.
•The ventricular 'escape‘ rhythm
has wide QRS complexes and
abnormal T waves. No further
interpretation of the ECG is
possible.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads V2-V4
•Raised ST segments in leads V2-
V4
•Inverted T waves in leads I, VL,
V2-V6

Clinical interpretation
Classic acute anterior myocardial
infarction.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Peaked P waves, best seen in lead
II
•Right axis deviation
•Dominant R waves in lead Vj
•Deep S waves in lead V6
•Inverted T waves in leads II, III, VF,
V1-V3
Clinical interpretation
•This combination of right axis
deviation, dominant R waves in lead
Vl and inverted T waves spreading
from the right side of the heart,
•is classical of severe right
ventricular hypertrophy.

4 thSymCARD 2014
The ECG shows:
•Atrial fibrillation with a ventricular
rate of about 40/min
•Left axis
•Left bundle branch block

Clinical interpretation
•When an ECG shows left bundle
branch block, no further
interpretation is usually possible.
Herethere is atrial fibrillation, and
the ventricular response is very
slow, suggesting that there is
conduction delay in the His bundle
as well as the left bundle branch.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Small Q waves in lead III but not
elsewhere
•Elevated ST segments in leads II,
III, VF, with upright T waves
•T wave inversion in lead VL
•Suggestion of ST segment
depression in leads V2-V3

Clinical interpretation
•A classic ECG of an acute inferior
myocardial infarction, with lead VL
indicating ischaemia. The rate of
development of Q waves is very
variable

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads II, III, VF
•Normal QRS complexes in the
anterior leads
•Marked ST segment elevation in
leads V1-V6

Clinical interpretation
•The Q waves in leads III and VF
suggest an old inferior infarction,
while the elevated ST segments in
leads V1-V6 indicate an acute
anterior infarction.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•PR intervals markedly prolonged
(480 ms)
•Normal axis
•Normal QRS complexes
•T wave inversion in leads V1-V3
Clinical interpretation
First degree block associated with
a non-Q wave anterior myocardial
infarction.

4 thSymCARD 2014
The ECG shows:
•Broad-complex tachycardia, rate
about 250/min
•Regular QRS complexes
•QRS duration 200 ms
•Indeterminate axis and QRS
configurations

Clinical interpretation
•In the context of acute myocardial
infarction, broad-complex
tachycardias should be considered
to be ventricular in origin unless the
patient is known to have bundle
branch block when in sinus rhythm.
Here the regularity of the rhythm
and the very broad complexes of
bizarre configuration leave no room
for doubt that this is ventricular
tachycardia.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads V2-V4
•Raised ST segments in leads V2-
V4
•Inverted T waves in leads I, VL,
V2-V6

Clinical interpretation
Classic acute anterior myocardial
infarction.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads V2-V4
•Raised ST segments in leads V2-
V4
•Inverted T waves in leads I, VL,
V2-V6

Clinical interpretation
Classic acute anterior myocardial
infarction.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads V2-V4
•Raised ST segments in leads V2-
V4
•Inverted T waves in leads I, VL,
V2-V6

Clinical interpretation
Classic acute anterior myocardial
infarction.

4 thSymCARD 2014
The ECG shows:
•Sinus rhythm
•Normal axis
•Q waves in leads V2-V4
•Raised ST segments in leads V2-
V4
•Inverted T waves in leads I, VL,
V2-V6

Clinical interpretation
Classic acute anterior myocardial
infarction.

4 thSymCARD 2014